Evidence map›Paper›PMID 27337457›Full record

ReviewMicrobiology spectrum2016

Macrophage Proresolving Mediators-the When and Where.

Jesmond Dalli, Charles Serhan

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Microbiology spectrum, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
8.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

69 citing papers in PubMed, 114 citations in OpenAlex.

  1. Trial
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  10. Article
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  14. Metabolic reprogramming in efferocytosis.Frontiers in cell and developmental biology · 2025
    Review
  15. Review
  16. Review
  17. Review
  18. Innate Immune Training Initiates Efferocytosis to Protect against Lung Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  19. Review
  20. Article

9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Jesmond DalliCenter for Experimental Therapeutics and Reperfusion Injury, Harvard Institutes of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115.
Charles SerhanCenter for Experimental Therapeutics and Reperfusion Injury, Harvard Institutes of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115.
Brigham and Women's Hospital · USHarvard University · US

Funding

Resolution Mechanisms in Acute Inflammation: Resolution PharmacologyP01GM095467 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 2011 to 2020
$14.8M
BLOOD CELL LIPOXYGENASE PRODUCTS: FORMATION AND ACTIONR01GM038765 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 1992 to 2020
$4.9M
NIGMS NIH HHS P01 GM095467NIGMS NIH HHS R01 GM038765
6 · The paper itself

Abstract

Macrophages and neutrophils orchestrate acute inflammation and host defense as well as the resolution phase and return to homeostasis. In this article, we review the contribution of macrophages to local lipid mediator (LM) levels and the regulation of macrophage LM profiles by polymorphonuclear neutrophils and neutrophil-derived microparticles. We carried out LM metabololipidomics, profiling distinct phagocytes: neutrophils (PMNs), apoptotic PMNs, and macrophages. Efferocytosis increased specialized proresolving mediator (SPM) biosynthesis, including resolvin D1 (RvD1), RvD2, and RvE2, which were further elevated by PMN microparticles. In studies using deuterium-labeled precursors (d8-arachidonic acid, d5-eicosapentaenoic acid, and d5-docosahexaenoic acid), apoptotic PMNs and microparticles contributed to SPM biosynthesis during efferocytosis. Assessment of macrophage LM profiles in M2 macrophages demonstrated higher SPM levels in this macrophage subset, including maresin 1 (MaR1), and lower amounts of leukotriene B4 (LTB4) and prostaglandins than in M1. Apoptotic PMN uptake by both macrophage subtypes led to modulation of their LM profiles. LTB4 was downregulated in M2, whereas SPMs including lipoxin A4 were increased. Conversely, uptake of apoptotic PMNs by M2 macrophages reduced (∼25%) overall LMs. MaR1 displays potent tissue-regenerative and antinociceptive actions in addition to its proresolving and anti-inflammatory actions. In addition, the MaR1 biosynthetic intermediate 13S,14S-epoxy-maresin is also bioactive, inhibiting LTB4 biosynthesis and switching macrophage phenotypes from M1 to M2. Together, these results establish LM signature profiles of human phagocytes and related subpopulations. They demonstrate microparticle regulation of macrophage-specific endogenous LMs during defined stages of acute inflammation and their dynamic changes in human primary phagocytes.

Indexed as

Lipid MetabolismAnimalsCell-Derived MicroparticlesHumansInflammation MediatorsMacrophagesNeutrophilsInflammation Mediators

Identifiers

PMID27337457
PMCPMC4922532
OpenAlexW2473681996

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.